"The Anabolic Androgenic Steroid Nandrolone Decanoate Disrupts Redox Homeostasis in Liver, Heart and Kidney of Male Wistar Rats"
http://www.plosone.org/article/infodoi10.1371journal.pone.0102699- it increased NADPH oxidase levels & activity in the heart and liver
- it decreased catalase and superoxide dismutase in the liver
- it decreased catalase in the kidney
- it reduced thiol residues
This essentially means that DECA administration increases oxidative damage via concomitant increase in production of the superoxide radical and a decrease in the activity of a couple of different endogenous antioxidants.
This study basically gives some mechanistic insight into exactly how AAS use can contribute to tissue damage that is sometimes seen
Maybe I'm wrong for even thinking like this, however, perhaps this implies that small doses.. such as slightly above normal levels (obviously normal levels imply, but maybe SLIGHT supraphysiological levels would be best), it would induce a mitohormetic response, augmented lifespan/longevity via these same outlined mechanisms. This study and a study cited in this paper note that the ROS prod is overproduced w/ respsect to the activity of the antioxidant systems.. however, smaller amounts of ROS signaling and general body stressors and can often induce mitohormesis, whereby your body becomes more robustly stress resistant by ramping up antioxidant defense capacities through a positive ROS signaling. This could also explain why men that go on TRT-esque doses most often become healthier.
My hypothesis may be supported by a few studies too:
"Testosterone increases renal anti-aging klotho gene expression via the androgen receptor-mediated pathway."
http://www.ncbi.nlm.nih.gov/pubmed/25163025&
"The Neuroprotective Effect of Klotho is Mediated via Regulation of Members of the Redox System"
http://www.jbc.org/content/early/2014/07/18/jbc.M114.567321Thus, testosterone - androgen receptor interaction signaling induces expression of the anti-aging gene/protein Klotho.. and Klotho is known to exert much of its protective and longevity benefitting effect through the redox system, the same one that is disrupted in the study from very high doses. Notwithstanding, perhaps the positive effects of AAS/testosterone are mediated most optimally, already, at the normal physiological level.
The psycho-social benefits of TRT and the nominal increases in strength/reported vitality and sexual function (in "low-dose" [i.e., not UFC] trials) seem to support something along the lines you suggest, although it really only suggests that systemic pathways are being improved. So, I think it would be an interesting area of research. Klotho seems to locate at least one interesting avenue of research.
Whereas the rat study you posted is no suprise and will probably get quoted by a trillion MDs, and conservative docs may overlook potential for normal-dose TRT to do some good. I've been interested in studies on TRT and while they're currently administered (ehhhh supposed to be administered) to low-test aging guys, it seems to me that research may soon support extended administration.